The results revealed that the expression of miR‑145 was significantly (P<0.05) downregulated in colon adenocarcinoma cells and the ectopic expression of miR‑145 in colon cancer inhibited proliferation by promoting the apoptosis of SW480 primary colon adenocarcinoma cells.
Knockdown of lincRNA-ROR restored the expression of miR-145, and had a significant influence on colon cancer cell proliferation, migration and invasion.
Herein, we study a PLGA/PEI (poly (d, l-lactide-co-glycolide)/polyethylenimine)-mediated miRNA vector delivery system; the validation of the method was carried out using a colon cancer xenograft model with miR-145 vector encoding for the expression of miR-145 (pDNA).
Our findings demonstrated that miR-145 and miR-1 play a negative regulatory role in the proliferation of colon cancer by targeting NAIP; thus, miR-145 and miR-1 may prove to be novel therapeutic targets in the treatment of colon cancer.
Most notable associations were for hsa-miR-145-3p [hazard ratio (HR) 2.94, 95% confidence interval (CI) 1.54, 5.61], and hsa-miR-9-3p (HR 10.28, 95% CI 1.31, 80.84) with colon cancer and hsa-miR-335-5p (HR 0.17, 95% CI 0.05, 0.54) for rectal cancer. hsa-miR-374a-5p, hsa-miR-570-3p and hsa-miR-18a-5p significantly reduced the hazard of dying for all cases, regardless of tumor site.
The aim of this study was to examine the expression pattern of the miR-17-92 cluster (miR-17, miR-18, miR-19, miR-20 and miR-92) as well as miR-21, miR-31, miR-135b, and miR-145 in early clinically diagnosed colon cancer.
Our current observations suggest that miR-21, miR-145, and their networks play critical roles in regulating CSCs growth and/or differentiation in the colon cancer and progression of chemo-resistance.
Taken together, these data suggested that miR-145 plays a pivotal role in colon cancer through inhibiting cell proliferation migration and invasion, and miR-145 may serve as a tumor suppressor by targeting paxillin gene.
microRNA‑145 (miR‑145) has been reported to be frequently downregulated in various types of cancer, including renal, prostate, bladder, lung and colon cancer, as well as B‑cell malignancies.
miR-143 and miR-145 are believed to function as colon cancer tumor suppressors, as they inhibit colon cancer cell growth and are downregulated in sporadic colonic tumors.
Using SILAC, we identified over 2000 proteins after reintroduction of miR-143 and miR-145, in the colon cancer cell line SW480, individually, and then, in concert.
Our findings show that chemically unmodified miRNAs complexed with PEI can be used in an efficient and biocompatible strategy of miRNA replacement therapy, as illustrated by efficacious delivery of PEI/miR-145 and PEI/miR-33a complexes in colon carcinoma.
An IGF-IR resistant to miR145 (again by elimination of its 3' UTR) is not down-regulated by miR145 but fails to rescue colon cancer cells from growth inhibition.